For more than 20 years, our understanding of the biology of atherosclerosis has incorporated the so-called inflammatory hypothesis. 1,2 Inflammatory cells and signals drive the healing response to vascular injury, allowing the initiation and growth of atherosclerotic plaque. Inflammatory reactions probably increase plaque instability, possibly resulting in plaque rupture, fissuring, or erosion and setting up the substrate for the thrombotic response that causes myocardial damage or infarction. Yet, no strictly antiinflammatory drugs are used to treat patients with coronary artery disease. Effective cardiovascular drugs with antiinflammatory effects, such as aspirin and statins, predominantly exert therapeutic benefits by means of mechanisms other . . .